In reply to all of what I read, I just want to add my two cents, pertaining
to Cl channels and inhibitory synapses!
In many (most?) neurons, the resting potential is close to the reversal
potential for Cl. So, through the opening of Cl channels by GABA or
whatever, the membrane can be hyperpolarized 5-10 mV. However, this slight
hyperpolarization is only partly responsible for the inhibition of a
saltatory conductance.
The main reason for the inhibition is that if the neuron's conductance is
wickedly increased to Cl then the neuron is effectively shunted, or clamped
near the reversal potential of Cl. Make sense?
Normally, if a neuron reaches threshold, meaning voltage-sensitive Na
channels open and the membrane hyperpolarizes due to an influx of Na, then
we have an action potential. But, if at this time of Na influx there is a
large Cl conductance increase, Cl will enter the neuron as Na enters,
thereby inhibiting an action potential (there will be no large change in
the cells potential difference).
Further, at the systems level, a large decrease of synaptic transmission in
various brain regions could have dire consequences.
-Fred Livingston